Descriptions

An increased metabolic efficiency may be a factor underlying the
onset and maintenance of obesity. This study examined the Resting
Metabolic Rate (RMR), the Thermic Effect of Food (TEF), the Thermic
Effect of Exercise (TEE), and the Potentiation (P) of the TEF by
Exercise in Juvenile-onset type obesity (JOTO), and Maturity-onset type
obesity (MOTO). It was hypothesized that individuals categorized as
JOTO would exhibit a greater metabolic efficiency and that this fact
would necessitate a differential diagnosis and treatment schema.
The RMR's of eight Juvenile-onset obese and eight Maturity-onset
obese middle aged women were measured for five minutes every half hour
for four hours under four conditions: 1) R-postabsorptive, 2) RF-postprandial,
3) RE-postabsorptive--exercised, and 4) RFE-postprandial--
exercised. Metabolic measurements were made via the technique of
indirect open circuit calorimetry.
The TEF (derived from integrating the total area under the 4 hour
response curve) was 40.8 Kcal and 31.5 Kcal for the JOTO and MOTO
subjects, respectively. The TEF after exercise amounted to 36 Kcal
for the JOTO individuals and 34 Kcal for the MOTO individuals. These
increases were significant (p<.001) compared to the baseline (R). The
energy expenditure was not significantly elevated following the
Exercise (RE) condition. JOTO individuals realized a 6.4 Kcal increase
while the energy expenditure increased by 4.7 Kcal for the MOTO
individuals.
These results suggest that the capacity for Juvenile-onset and
Maturity-onset obese women to respond to thermogenic stimulation is
essentially the same. No significant differences were apparent between
these groups on any of the measures of metabolic efficiency. This is
not to say, however, that metabolic efficiency is not an underlying
factor in the development and persistence of the obese state. Both
groups displayed a subnormal response to the food stimulus. Moreover,
exercise after eating failed to potentiate the TEF as it does in lean
individuals.
These blunted metabolic responses may constitute a partial
explanation for the etiology of obesity and may provide a rationale for
a more enlightened therapeutic approach. Possible mechanisms for this
blunted metabolic response might be a limited capacity to elevate
metabolic rate, a reduced sensitivity to the neural and hormonal
stimulation afforded by food and exercise, and a reduced rate of substrate
cycling.